磷酸肌酸对新生鼠缺氧缺血性脑损伤线粒体功能的影响

Effect of Phosphocreatine on Mitochondrial in Brain Tissue of Neonate Rats After Hypoxia Ischemia Brain Damage(HIBD)

目的:探讨外源性磷酸肌酸(PCr)在缺氧缺血性脑损伤中对线粒体功能的影响。方法:将96只七日龄Wistar新生鼠随机分为四组,分别为A假手术组、B生理盐水对照组、C磷酸肌酸小剂量干预组、D磷酸肌酸大剂量干预组,每组24只。除假手术组外其余三组动物制成HIBD模型,并在术前1h分别给予生理盐水、小剂量磷酸肌酸、大剂量磷酸肌酸腹腔注射,24h后取脑,观察脑组织线粒体内三磷酸腺苷(ATP)、还原型谷胱甘肽(GSH)以及丙二醛(MDA)的含量变化。结果:外源性磷酸肌酸干预后脑组织中线粒体内ATP、GSH、MDA含量与盐水对照组相比具有差异性(P<0.05)。结论:外源性磷酸肌酸可以改善线粒体能量代谢,减轻脂质过氧化,保护脑组织。

Objective： To observe the effect of exogenous phosphocreatine on the level changes of S100b protein and NSE In serum with serious hypoxia -ischemic encephalopathy in newborn infants. Methods： 40 serious asphxia newborn were randomly devided into two groups： routin therapy group（21 newborns）, routin treatment with oxygen ,nutrition and citicoline（CTL）.The treatment group（19 newboms） were given exogenous phosphocreatine （12h after born, 1 g/d） besides conventional therapy which was given in control only. The control group （14 newborn）without asphyxia newborns. The content of S100b protein and NSE in serum were measured using enzyme-linked immuradsorbent assay （ELISA） after 48h and 10 days. The newborns in both groups were assessed with neurological fimction, the NABA scores was recorded. Results： The level of NSE and S100B protein In serum in the treatment group and routin theray group in 48h were no significantly difference （ ※P〉0.05, ※P〉0.05）. As compared with control group it was significantly difference （ △P〈0.05,△P〈0.05 ）. The level of NSE and S-100B protein In serum after 10 days between two group were significantly difference, the treatment group were significantly decreased （※P〈0.05, ※P〈0.05）. The NBNA score〈 35 point after 3 weeks account for 27.0% in treatment group and 53% in control group,which had significantly difference （x2=6.112, ※P〈0.05）. Conclusions： Exogenous phosphocreatine can protect brain tissure and improve the energetic metabolism of the brain cell, can lessen cerebral ischemic injury,which can decrease disability rate and improve neurological function.